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MBBS 4 Dermatology > Bacterial Cutaneous Infections > Flashcards

Bacterial Cutaneous Infections Flashcards

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1
Q

How is the skin a physical and immunological barrier?

A
  1. physical
    - tough epidermal cover
  2. immunological
    - Cytokines, antimicrobial peptides, complement
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2
Q

Classification of bacterial skin infections?

A
  1. Primary infections (pyoderma) of the skin itself
  2. Secondary infections: on existing dermatoses
    e.g. impetiginisation in AD lesions or ulcer
  3. Skin lesions manifesting in the presence of systemic infection
    e.g. skin lesions in acute generalized miliary TB.
  4. Reactive changes resulting from distant infection
    e.g. Osler’s nodes and petechiae of subacute bacterial endocarditis.
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3
Q

What is impetigo?

A

infection of the epidermis just under the stratum corneum (subcorneal layer of epidermis)
- usually with staphylococcus aureus or streptococcus pyogenes

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4
Q

Folliculitis?

A

infection of the mouth of the hair follicle

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5
Q

Ecthyma?

A

infection of full thickness of epidermis

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6
Q

Boil?

A

abscess of hair follicle

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7
Q

Carbuncle?

A

abscess of several adjacent hair follicles

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8
Q

Erysipelas?

A

infection of the upper half of the dermis

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9
Q

Cellulitis?

A

infection of the lower half of the dermis

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10
Q

Necrotizing fasciitis?

A

infection of the subcutaneous fat and deep fascia

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11
Q

For every skin infection you should consider?

A

Portal of entry
1. Look for existing break in the skin
e.g. excoriations, insect bites, ulcers, primary dermatoses (tinea pedis, A.D) etc
2. Prematurity in case of young child.

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12
Q

What is the main cause of superficial skin infections?

A

staphylococcal infections
- Superficial pyodermas affect the epidermis; just below s.corneum or in hair follicles.
Note: If untreated, can extend into the dermis resulting in ecthyma and furuncle formation respectively

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13
Q

Name the superficial skin infections?

A
  1. impetigo
  2. ecthyma
  3. abscess
  4. furuncle
  5. carbuncle
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14
Q

Describe impetigo?

A
  • infection of subcorneal layer of epidermis
  • Common in children
  • highly contagious
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15
Q

2 clinical patterns of impetigo?

A
  1. Bullous
  2. Non-bullous
    - S.aureus causes both patterns, but group A Streptococci common cause in developing countries
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16
Q

Describe bullous impetigo?

A
  • Exfoliative toxin A from s. aureus cleaves desmoglein to form bulla.
  • Common in neonates and sometimes older infants
  • Vesicles rapidly progress to flaccid bullae
  • Bullae are well defined, clear, non-erythematous surrounding.
  • Rupture after 1-2 days, results yellow crusts
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17
Q

Describe non bullous impetigo?

A
  • Most common, 70% of impetigo
  • Common around the face (nares and perioral), & extremities after trauma.
  • Clinical: vesicle/pustule that quickily becomes crusted plaque (honey colored crust).
  • Usually red halo.
  • Ecthyma results if untreated, but spontaneous resolution also possible
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18
Q

What is characteristic of bullous impetigo?

A

vesicles rapidly coalesce to form flaccid bullae

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19
Q

Describe ecythma?

A
  • Thickly crusted erosions/ulcerations.
  • Can evolve from primary pyoderma, within existing dermatoses or at site of trauma.
  • Poor hygiene and neglect key in its development.
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20
Q

Ddx of bullous impetigo?

A
  1. dermatitis
  2. bullous insect bites
  3. bullous tinea
  4. bullous fixed drug reaction
  5. SSSS
  6. thermal burns
  7. pemphigus vulgus
  8. bullous pemphigoid
  9. erythema multiforme
  10. dermatitis herpetiformis
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21
Q

What do you always rule out in bullous impetigo?

A
  1. herpes simplex
  2. varicella
  3. bullous tinea
  4. bullous fixed drug reaction
  5. bullous drug reaction
  6. SSSS
22
Q

Ddx of non-bullous impetigo?

A
  1. seborrheic dermatitis
  2. atopic dermatitis
  3. allergic contact dermatitis
  4. epidermal dermatophyte infections
  5. tinea capitis
  6. herpes simplex
  7. varicella
  8. herpes zoster
  9. scabies
  10. pediculosis capitis
23
Q

What do you rule out in non-bullous impetigo?

A
  1. herpes simplex
  2. herpes zoster
  3. scabies
24
Q

General management of impetigo?

A

Hygiene: cleaning hands in between at risk patients (e.g. pediatric nurseries) exam.

25
Q

Management of impetigo in mild and moderate cases?

A
  1. Clean and remove crusts.
  2. Topical antibiotics: mupirocin or fucidin ointments 2 or 3 times daily
  3. Wet dressings: PP soaks, GV paint
26
Q

Management of impetigo in severe or complicated cases?

A

Penicilin
e.g. amoxycillin/clavulinic acid (augmentin)
OR
Erythromycin
OR
IV ceftriaxon, IV ampicillin

27
Q

Describe an abscess?

A
  • collection of pus, walled off from sorrounding tissues.
  • present as painful, fluctuant mass.
  • Abscess can occur anywhere
28
Q

Describe a furuncle?

A
  • collection of pus, walled off from sorrounding tissues.
    present as painful, fluctuant mass.
  • if the collection involve hair follicle, it is furuncle
  • therefore occur in hair bearing areas only.
29
Q

Describe a carbuncle?

A
  • collection of furuncles extending into subcutaneous tissue
  • Multiple discharging sinuses on the surface
30
Q

Treatment of abscess/furuncle/carbuncle?

A
  1. Warm compresses and later drainage if mild
  2. Incision and drainage if fluctuant.
  3. Systemic antibiotics if
    - lesions around nares and external auditory canal.
    - large and/or recurrent.
    - associated with cellulitis
    - non responsive to conservative care.
31
Q

Name the deeper infections?

A
  1. erysipelas
  2. cellulitis
32
Q

Describe deeper infections?

A
  1. Include acute, tender, spreading, edematous suppurative inflammation of dermis, subcutaneous tissue and muscle.
  2. Often associated with fever, chills, local pain.
  3. Can present on
    - antecedent site; ulcer, insect bites, dermatitis,
    - Deeper tissue infection e.g. osteomyelitis
  4. Initially present with local pain and erythema.
33
Q

Describe erysipelas and cellulitis?

A
  1. ERYESIPELAS: involves upper dermis
  2. Cellulitis involves deep dermis and SC tissues.
    - may be associated with lymphangitis, presenting as a red streak leading to lymph node.
34
Q

Causes of erysipelas and cellulitis?

A
  1. Grp A streptococcus and s. aureus common causes.
  2. Hemophilus influenza, E.coli
35
Q

Risk factors for erysipelas and cellulitis?

A
  1. DM,
  2. peripheral vascular disease
  3. lymphedema
  4. chronic cutaneous ulcers
  5. the very young
  6. the aged
  7. HIV
  8. tinea pedis
  9. obesity
  10. IV drug abuse
36
Q

Clinical features of erysipelas?

A
  1. Pain, erythema and plaque like edema (peau d’orange), that is rapidly progressing
  2. Usually preceded by abrupt onset of fever, chills, malaise and nausea.
  3. Overlying edema on involved site clearly demarcates it from normal surrounding.
  4. May result in blistering
  5. Common on lower limbs and Face
37
Q

Complications of erysipelas?

A
  1. Thrombophlebitis
  2. Necrotizing fascitis & abscess
  3. Acute glomerulonephritis
  4. Subacute bacterial endocarditis
  5. Damaged lymphatics => recurrence (prophylactic AB may be necessary, therapeutic elastic stockings)
38
Q

Clinical features of cellulitis?

A
  1. Pain, erythema and plaque like edema (peau d’orange), that is rapidly progressing
  2. Usually preceded by abrupt onset of fever, chills, malaise and nausea.
    has less distinction with sorrounding normal skin, with non-palpable borders
  3. May result in blistering
  4. Common on lower limbs and Face
39
Q

Predisposing factors to cellulitis?

A
  1. Immunocompromised hosts
  2. Diabetic ulcers
  3. Decubitus ulcers
  4. Chronic venous insufficiency
  5. Alcoholics
  6. Malignancy
  7. I.V drug abusers
  8. Peripheral vascular disease
40
Q

What is gangrenous cellulitis?

A
  • Process in the superficial and/or deep fascia with secondary changes on the skin.
  • erythema, bulla formation & frank necrosis (incl. myonecrosis)
41
Q

Characteristic features of gangrenous cellulitis?

A

Characterised by rapidly developing, progressive disease
1. Constitutional symptoms
2. severe pain and tenderness invariably present.

42
Q

Clinical features of necrotizing fasciitis?

A
  1. Common in extremities, abdominal wall or around operative wounds.
  2. May be preceded by deceptively small area of cutaneous involvement.
  3. Progression from erythema, pain, edema through bullae formation to full necrosis of overlying skin
  4. may be rapid and dramatic, exposing tendons and muscle
  5. Pain may subside at this point due to destruction of subcutaneous nerves
43
Q

Name and describe other variants of gangrene?

A
  1. Fournier’s Gangrene: localised variant with necrosis of scrotum and penile shaft.
  2. Gas Gangrene: due to gas `forming C. pefringens.
44
Q

Treatment of mild erysipelas and cellulitis?

A
  1. Immobilise, wet dressing
  2. Medical therapy
    - Oral peniciliin (dicloxacillin)
    - Oral Penicillin V
    - Erythromycin/Clindamycin in penicillin allergy
45
Q

Treatment of severe erysipelas and cellulitis?

A
  1. High dose IV penicillin.
  2. cephalosporin
46
Q

Treatment of necrotising cellulitides?

A
  1. high dose IV antibiotics
    AND
  2. early and extensive debridement of the necrotic tissues
    - Prognosis generally poor
47
Q

What is anthrax?

A
  • fatal disease in livestock and wild herbivores
  • Humans are usually infected incidentally
  • Most human disease is cutaneous,followed by oral-pharyngeal
  • Gastrointestinal and inhalational
  • Disease is mediated through toxins which cause edema,
  • Hemorrhage, and necrosis
  • Mortality rate is high
48
Q

Anthrax diagnosis?

A
  1. clinical
  2. biopsy
  3. gram stain
  4. culture
  5. serology
49
Q

Anthrax treament?

A
  1. penicillin
  2. ciprofloxacin,
  3. tetracycline
  4. erythromycin
  5. chloramphenicol
  6. streptomycin
50
Q

Anthrax prevention?

A
  1. vaccination or quarantine of animals
  2. destruction of animal products
    - Antrax spores survive for years in dry soil!!!
  3. Persons who work with animal products(hides) have been infected
51
Q

Anthrax pathogenesis?

A
  1. Entering the skin anthrax spores germinate forming:
    - a malignant pustule :production toxine
    - generalised edema
  2. Inhalation results in phagocytosis of spores by macrophages
    - death due to primary pneumonia
  3. Ingestion of meat :ulceration and haemorrhage
    - at the point of entry in the submucosa
    - Hemorrhagic meningitis can result from bacteremia

MBBS 4 Dermatology (21 decks)

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